2. Some of the conditions prejudicial to the maintenance of an optimum cellular reserve in the infected animal have been revealed; viz., undernutrition, physical cold, intratracheal route of infection.

3. The potential threat exerted by latent foci of streptococci, and the importance, in relation to the combined infection with virus, of cellular and humoral immunity, together or separately, have been demonstrated. The essential rôle of optimum nutrition (notably as concerns the vitamin B complex, and folic acid specifically) in the prevention of disastrous illness from these infectious agents, individually or in combination, would seem to have been proven.

4. Signs of glomerular nephritis appeared in a significant number of monkeys receiving Streptococcus hemolyticus and influenza virus in sequence, followed by reinoculation or spontaneous reappearance of the streptococci.

5. Reinoculation of Streptococcus hemolyticus, group C, resulted in a prompt "booster" increase in the opsonic index. Virus instillation was followed by just as sudden a depression in this index.

6. Reinoculation failed to evoke either the granulocytosis or the leucopenia in monkeys which are characteristic effects of the streptococcus and the virus respectively when these agents are introduced for the first time by way of the nasal mucous membrane.

7. Simultaneous intranasal inoculation of influenza virus, type A, and Streptococcus hemolyticus, group C, in nutritionally normal Macaca mulatta failed to produce obvious signs of disease. In most of the animals, however, a streptococcus-induced leucocytosis followed by a delayed virus-induced granulopenia developed.

8. Inoculation of influenza virus followed in 4 to 17 days by streptococci produced obvious signs of disease in five of eleven animals which had become leucopenic as result of the action of the virus, and fatal streptococcal septicemia in two monkeys.

9. The development of signs of infection in previously healthy monkeys exposed to virus followed by streptococci confirms both the clinical and laboratory experience of other observers, that virus infection may predispose to secondary bacterial invasion, and, that at times, under unfavorable circumstances, the infection may become overwhelming. Although the complete mechanism of resistance is as yet not wholly clear, the depressant or inhibitory effect of the virus on both its cellular and humoral elements has been established.